Cholesterol

evidence_access

Primary full text

experimental_model

Pharmacologically altered lysosomal cholesterol handling.

limitations

Not evidence that raising blood cholesterol or dietary cholesterol protects the lung.

nutrient_topic

Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon

plain_language

Membrane-lipid handling can modify the response to particles.

primary_references

Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180

Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 496–502

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Pharmacologically altered lysosomal cholesterol handling. · source_derived_draft · unverified_draft

## silica-cholesterol-lysosome Membrane-lipid handling can modify the response to particles. U18666A-induced cholesterol accumulation reduced silica-induced inflammasome activation in mouse alveolar macrophages. Model: Pharmacologically altered lysosomal cholesterol handling. Limitations: Not evidence that raising blood cholesterol or dietary cholesterol protects the lung. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180

evidence_span

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experimental_model

Cryo-EM, binding, cell assays and molecular dynamics

exposure

Apo, osteocalcin-bound and vitamin-K-bound structures

limitations

Shared vitamin K chemistry; the abstract does not establish K2 exclusivity or identical kinetics for every menaquinone.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human GGCX

plain_language

Membrane cholesterol is part of the enzyme environment, not just an unrelated blood measurement.

primary_references

[k2-p39880952] Structure and mechanism of vitamin-K-dependent γ-glutamyl carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39880952/ DOI: 10.1038/s41586-024-08484-9

tissue_or_cell_type

Endoplasmic-reticulum membrane enzyme

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 396–407

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM, binding, cell assays and molecular dynamics · source_derived_draft · unverified_draft

### k2-ggcx-cholesterol A cholesterol molecule interacted with GGCX transmembrane helices; structural, cellular and simulation results connected this site with regulation of cellular GGCX protein levels. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Membrane cholesterol is part of the enzyme environment, not just an unrelated blood measurement. organism: Human GGCX tissue_or_cell_type: Endoplasmic-reticulum membrane enzyme experimental_model: Cryo-EM, binding, cell assays and molecular dynamics limitations: Shared vitamin K chemistry; the abstract does not establish K2 exclusivity or identical kinetics for every menaquinone. exposure: Apo, osteocalcin-bound and vitamin-K-bound structures evidence_span: {"source_cache": "artifacts/k2-research/39880952.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653", "start_char": 0, "end_char": 1230, "text_sha256": "eb8e6d00eecd7c5c780921cae3f804fab60e919301eeb16e9909f36293aaa653"} [k2-p39880952] Structure and mechanism of vitamin-K-dependent γ-glutamyl carboxylase. (2025). https://pubmed.ncbi.nlm.nih.gov/39880952/ DOI: 10.1038/s41586-024-08484-9

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Observational comparison of 85 cirrhosis and 50 noncirrhotic liver-disease patients

exposure

Absolute vitamin E compared with vitamin E/cholesterol ratio using study-specific healthy-control reference limits.

limitations

No direct tissue adequacy test. Cirrhosis changes lipid handling; neither an absolute concentration nor a normalized ratio alone establishes cellular function.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Lipid correction is useful context, but it can also conceal a problem when liver disease changes both measurements.

primary_references

[e-clin-cirrhosis1999] Vitamin E status in patients with liver cirrhosis: normal or deficient? (1999). https://pubmed.ncbi.nlm.nih.gov/9920150/ DOI: 10.1016/s0026-0495(99)90015-x

tissue_or_cell_type

Serum and liver-disease context

trigger_kind

biomarker_context Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1245–1256

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational comparison of 85 cirrhosis and 50 noncirrhotic liver-disease patients · source_derived_draft · unverified_draft

### e-clin-cirrhosis-ratio-boundary In the cirrhosis cohort, cholesterol normalization classified fewer patients as vitamin E deficient than absolute concentrations; the authors cautioned that the ratio could obscure reduced status in advanced liver disease. Condition category: biomarker_context nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lipid correction is useful context, but it can also conceal a problem when liver disease changes both measurements. organism: Homo sapiens tissue_or_cell_type: Serum and liver-disease context experimental_model: Observational comparison of 85 cirrhosis and 50 noncirrhotic liver-disease patients limitations: No direct tissue adequacy test. Cirrhosis changes lipid handling; neither an absolute concentration nor a normalized ratio alone establishes cellular function. exposure: Absolute vitamin E compared with vitamin E/cholesterol ratio using study-specific healthy-control reference limits. cross_nutrient: false [e-clin-cirrhosis1999] Vitamin E status in patients with liver cirrhosis: normal or deficient? (1999). https://pubmed.ncbi.nlm.nih.gov/9920150/ DOI: 10.1016/s0026-0495(99)90015-x

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Original patient-specimen laboratory analysis within an article indexed as review

exposure

Lipid-adjusted assessment; reference specimens n=307; low-concentration subset n=59.

limitations

Laboratory reclassification, not a direct tissue-deficiency gold standard. The abstract has an apparent typo in a separate high-concentration denominator; that statistic is not used here.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

A low vitamin E concentration can look different once blood lipids are considered.

primary_references

[e-clin-winbauer1999] Evaluating serum alpha-tocopherol (vitamin E) in terms of a lipid ratio. (1999). https://pubmed.ncbi.nlm.nih.gov/10440582/

tissue_or_cell_type

Serum

trigger_kind

biomarker_context Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1232–1243

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Original patient-specimen laboratory analysis within an article indexed as review · source_derived_draft · unverified_draft

### e-clin-lipid-ratio-reclassification Among 59 specimens with alpha-tocopherol below 5 mg/L, 28 were reclassified within the study lipid-ratio reference interval after cholesterol and triglycerides were considered. Condition category: biomarker_context nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low vitamin E concentration can look different once blood lipids are considered. organism: Homo sapiens tissue_or_cell_type: Serum experimental_model: Original patient-specimen laboratory analysis within an article indexed as review limitations: Laboratory reclassification, not a direct tissue-deficiency gold standard. The abstract has an apparent typo in a separate high-concentration denominator; that statistic is not used here. exposure: Lipid-adjusted assessment; reference specimens n=307; low-concentration subset n=59. cross_nutrient: false [e-clin-winbauer1999] Evaluating serum alpha-tocopherol (vitamin E) in terms of a lipid ratio. (1999). https://pubmed.ncbi.nlm.nih.gov/10440582/

cross_nutrient

true

experimental_model

Human NPC1L1 overexpression co-substrate assay

exposure

Cholesterol and alpha-tocopherol co-incubation; concentrations unavailable in abstract.

limitations

No dietary cholesterol threshold or universal supplement-spacing rule follows.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Human protein in cultured cells

plain_language

Cholesterol changed vitamin E uptake through their shared transporter.

primary_references

[narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034

tissue_or_cell_type

Cellular uptake model

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 220–231

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NPC1L1 overexpression co-substrate assay · source_derived_draft · unverified_draft

### ve-transport-npc1l1-cholesterol-competition Cholesterol inhibited human NPC1L1-mediated alpha-tocopherol uptake in mutual substrate-interaction experiments. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cholesterol changed vitamin E uptake through their shared transporter. organism: Human protein in cultured cells tissue_or_cell_type: Cellular uptake model experimental_model: Human NPC1L1 overexpression co-substrate assay limitations: No dietary cholesterol threshold or universal supplement-spacing rule follows. exposure: Cholesterol and alpha-tocopherol co-incubation; concentrations unavailable in abstract. cross_nutrient: true [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034

evidence_access

Primary abstract

experimental_model

Prostate-cancer experimental models.

limitations

Does not imply a testosterone-boosting effect of supplements or a human dietary cancer treatment.

nutrient_topic

L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine

plain_language

The pathway linked amino-acid carbon handling to lipid and hormone-related tumor adaptation.

primary_references

Isoleucine and valine promote prostate cancer progression via propionyl-CoA-mediated cholesterol metabolism. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42625032/ · DOI 10.1038/s42255-026-01583-z

L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 514–520

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Prostate-cancer experimental models. · source_derived_draft · unverified_draft

## isoleucine-prostate-cholesterol The pathway linked amino-acid carbon handling to lipid and hormone-related tumor adaptation. The reported SREBP2 activation promoted cholesterol biosynthesis and supported de novo androgen production and androgen-receptor signaling under metabolic/androgen-deprivation stress. Model: Prostate-cancer experimental models. Limitations: Does not imply a testosterone-boosting effect of supplements or a human dietary cancer treatment. Evidence access: Primary abstract Isoleucine and valine promote prostate cancer progression via propionyl-CoA-mediated cholesterol metabolism. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42625032/ · DOI 10.1038/s42255-026-01583-z

evidence_span

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experimental_model

Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate

exposure

Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients

limitations

The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response.

nutrient_topic

Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

organism

Human

plain_language

It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained.

primary_references

[bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025

tissue_or_cell_type

Monocyte

Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 463–474

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate · source_derived_draft · unverified_draft

### bg-mevalonate-not-cholesterol-trains Activation of the cholesterol synthesis pathway but not the synthesis of cholesterol itself is essential for training of myeloid cells, rather the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways, statins which block mevalonate generation prevent trained immunity induction, and monocytes of patients with hyper immunoglobulin D syndrome who are mevalonate kinase deficient and accumulate mevalonate have a constitutive trained immunity phenotype at both immunological and epigenetic levels. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained. organism: Human tissue_or_cell_type: Monocyte experimental_model: Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate limitations: The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response. exposure: Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients evidence_span: {"source_cache": "artifacts/glucan-research/29328908.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03", "start_char": 0, "end_char": 1173, "text_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03"} [bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025

evidence_access

Primary abstract

experimental_model

Human recombinant catalytic-domain crystallography and biochemical background.

limitations

Shared human machinery; the source is not an experiment administering red yeast rice.

nutrient_topic

Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice

plain_language

This enzyme supplies a shared precursor pathway.

primary_references

[10698924] Crystal structure of the catalytic portion of human HMG-CoA reductase: insights into regulation of activity and catalysis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10698924/ · DOI 10.1093/emboj/19.5.819

Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 76–82

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant catalytic-domain crystallography and biochemical background. · source_derived_draft · unverified_draft

## red-yeast-rice-human-mevalonate-machinery This enzyme supplies a shared precursor pathway. Human HMG-CoA reductase catalyzes mevalonate formation; substrate/cofactor-bound structures locate HMG-CoA and the nicotinamide cofactor in the catalytic domain. Model: Human recombinant catalytic-domain crystallography and biochemical background. Limitations: Shared human machinery; the source is not an experiment administering red yeast rice. Evidence access: Primary abstract [10698924] Crystal structure of the catalytic portion of human HMG-CoA reductase: insights into regulation of activity and catalysis. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10698924/ · DOI 10.1093/emboj/19.5.819

evidence_span

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experimental_model

GLUT4 trafficking, glucose uptake and cholesterol add-back experiments

exposure

Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation

limitations

Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Mouse 3T3-L1 adipocytes

plain_language

Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism.

primary_references

[chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255

tissue_or_cell_type

Cultured adipocyte plasma membrane

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 328–339

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft

### chromium-cholesterol-dependent-uptake Chromium-associated membrane-cholesterol reduction accompanied enhanced insulin-stimulated glucose uptake, and cholesterol add-back prevented the trafficking and uptake benefit. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Putting cholesterol back into the membrane removed the effect, supporting a membrane-dependent mechanism. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255

evidence_span

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experimental_model

Hyperinsulinemia model with AMPK silencing

exposure

Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA

limitations

Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Rat L6 skeletal muscle myotubes

plain_language

The treatment prevented a membrane-lipid change associated with insulin resistance in this model.

primary_references

[chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007

tissue_or_cell_type

Cultured muscle plasma membrane and cortical actin

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 367–378

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft

### chromium-membrane-cholesterol-protection Chromium picolinate protected hyperinsulinemic L6 myotubes against excess membrane cholesterol. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treatment prevented a membrane-lipid change associated with insulin resistance in this model. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007

evidence_access

Primary abstract

experimental_model

Male C57BL/6J diet-induced obesity; rebaudioside A and vehicle comparators.

limitations

Mouse dosing is not ordinary human food exposure; lower lipid content does not identify a unique molecular target.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

A less common glycoside had a liver phenotype in an obesity model.

primary_references

Rebaudioside D decreases adiposity and hepatic lipid accumulation in a mouse model of obesity. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38321177/ · DOI 10.1038/s41598-024-53587-y

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 418–424

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male C57BL/6J diet-induced obesity; rebaudioside A and vehicle comparators. · source_derived_draft · unverified_draft

## stevia-rebd-liver A less common glycoside had a liver phenotype in an obesity model. Rebaudioside D at 50 mg/kg orally for 12 weeks reduced hepatic triglycerides, cholesterol and lipid peroxidation in male high-fat/high-sucrose-fed mice. Model: Male C57BL/6J diet-induced obesity; rebaudioside A and vehicle comparators. Limitations: Mouse dosing is not ordinary human food exposure; lower lipid content does not identify a unique molecular target. Evidence access: Primary abstract Rebaudioside D decreases adiposity and hepatic lipid accumulation in a mouse model of obesity. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38321177/ · DOI 10.1038/s41598-024-53587-y

evidence_span

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experimental_model

Randomized crossover comparisons of pectin preparations

exposure

15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator

limitations

Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

The response was not unique to citrus pectin.

primary_references

[pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208

tissue_or_cell_type

Circulating lipids

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 776–787

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover comparisons of pectin preparations · source_derived_draft · unverified_draft

### pectin-ldl-apple Apple DE70 pectin also reduced LDL in the 15-g/day study. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response was not unique to citrus pectin. organism: Homo sapiens tissue_or_cell_type: Circulating lipids experimental_model: Randomized crossover comparisons of pectin preparations limitations: Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference. exposure: 15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator evidence_span: {"source_cache": "artifacts/pectin-research/22190137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611", "start_char": 0, "end_char": 1601, "text_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611"} [pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208

evidence_span

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experimental_model

Randomized crossover comparisons of pectin preparations

exposure

15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator

limitations

Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

The pectin preparation influenced the cholesterol result.

primary_references

[pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208

tissue_or_cell_type

Circulating lipids

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 763–774

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover comparisons of pectin preparations · source_derived_draft · unverified_draft

### pectin-ldl-citrus Citrus DE70 pectin reduced LDL by approximately 7-10% in the 15-g/day comparison, outperforming several other preparations. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pectin preparation influenced the cholesterol result. organism: Homo sapiens tissue_or_cell_type: Circulating lipids experimental_model: Randomized crossover comparisons of pectin preparations limitations: Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference. exposure: 15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator evidence_span: {"source_cache": "artifacts/pectin-research/22190137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611", "start_char": 0, "end_char": 1601, "text_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611"} [pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208

evidence_span

{"source_cache": "artifacts/pectin-research/22190137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611", "start_char": 0, "end_char": 1601, "text_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611"}

experimental_model

Randomized crossover comparisons of pectin preparations

exposure

15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator

limitations

Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

The trial also found an LDL response at its lower tested regimen.

primary_references

[pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208

tissue_or_cell_type

Circulating lipids

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 789–800

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover comparisons of pectin preparations · source_derived_draft · unverified_draft

### pectin-ldl-low-dose The tested high-molecular-weight DE70 citrus pectins at 6 g/day lowered LDL by approximately 6-7%. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial also found an LDL response at its lower tested regimen. organism: Homo sapiens tissue_or_cell_type: Circulating lipids experimental_model: Randomized crossover comparisons of pectin preparations limitations: Preparation-specific lipid surrogates; no cardiovascular event outcome. Methylesterification alone did not explain every preparation difference. exposure: 15 g/day for four weeks; additional high-MW citrus preparation at 6 g/day for three weeks; cellulose comparator evidence_span: {"source_cache": "artifacts/pectin-research/22190137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611", "start_char": 0, "end_char": 1601, "text_sha256": "20212c2dcb0b2018c37d0eac06932c1ec9da0a9d514bb3bd905f476594b32611"} [pectin-p22190137] Cholesterol-lowering properties of different pectin types in mildly hyper-cholesterolemic men and women. (2012). https://pubmed.ncbi.nlm.nih.gov/22190137/ DOI: 10.1038/ejcn.2011.208